Anesthesiology
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Patients undergoing coronary artery bypass graft (CABG) surgery frequently develop wall motion abnormalities diagnosed by intraoperative transesophageal echocardiography. However, the relation between deterioration in wall motion and postoperative morbidity or mortality is unclear. Therefore, the authors hypothesized that deterioration in intraoperative left ventricular regional wall motion immediately after CABG surgery is associated with a higher risk of adverse cardiac events. ⋯ The authors confirmed their hypothesis that deterioration in wall motion detected by intraoperative echocardiography after CABG surgery is associated with increased risk of long-term adverse cardiac morbidity. Worsening wall motion after CABG surgery should be considered a prognostic indicator of adverse cardiovascular outcome.
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Mechanical ventilation is delivered to sedated patients during anesthesia, but also to nonsedated patients (ventilator weaning, noninvasive ventilation). In these circumstances, patient-ventilator asynchrony may occur, provoking discomfort and unduly increasing work of breathing. In certain cases, it is associated with an increased inspiratory load. Inspiratory loading in awake humans activates the premotor cortical regions, as illustrated by the occurrence of electroencephalographic premotor potentials. In normal humans during noninvasive ventilation, the authors used an experimental model of patient-ventilator asynchrony to determine whether premotor cortical activation occurs in this setting. ⋯ This study indicates that "ventilator fighting" in healthy humans is associated with an activation of higher cerebral areas. Premotor potentials could thus be markers of patient-ventilator asynchrony at the brain level. Both corroboration in patients and the elucidation of the causative or reactive nature of the association are needed before determining clinical implications.
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Hydrocortisone protects against ischemia-reperfusion injury, reduces paracellular permeability for macromolecules, and is routinely applied in the prevention of interstitial edema. Healthy vascular endothelium is coated by the endothelial glycocalyx, diminution of which increases capillary permeability, suggesting that the glycocalyx is a target for hydrocortisone action. ⋯ Hydrocortisone preserves the endothelial glycocalyx, sustaining the vascular barrier and reducing interstitial edema. The effect of colloids suggests that prevention of postischemic rise in coronary resistance by hydrocortisone could also be based on alleviation of endothelial swelling. Stabilization of myocardial mast cells by hydrocortisone may account for the mitigated inflammatory affect of ischemia-reperfusion.
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Comparative Study
Cerebral air emboli differentially alter outcome after cardiopulmonary bypass in rats compared with normal circulation.
Cerebral air emboli (CAE) are thought to contribute to adverse cerebral outcomes following cardiac surgery with cardiopulmonary bypass (CPB). This study was designed to investigate the effect of escalating volumes of CAE on survival and neurologic and histologic outcomes. In addition, the effect of xenon administration during CAE on these outcomes was determined. ⋯ This study describes the successful incorporation of CAE in a rodent CPB model and allows identifying suitable CAE volumes for subsequent studies. CAE exhibit a differential effect on outcome in rats undergoing CPB versus those not exposed to CPB. Perioperative administration of xenon remained without any effect on outcome.
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Activation of A1 adenosine receptors (A1Rs) causes antinociception after nerve injury and inflammation. However, the role of A2a adenosine receptors (A2aRs) for pain processing is less clear. In the current study, the authors investigated the role of spinal adenosine A1Rs and A2aRs for the maintenance of mechanical hyperalgesia in an animal model for postoperative pain. ⋯ Spinal A1Rs but not A2aRs play an important role in the maintenance of nonevoked and evoked pain behaviors after an incision. Furthermore, A1R-induced spinal antinociception is mediated by interactions with pertussis toxin-sensitive G proteins. In addition, the opening of adenosine triphosphate-sensitive K channels but not of calcium-activated potassium channels and voltage-gated Kv1.3 or Kv1.6 channels contribute to the antinociceptive effect of A1R agonists.